Human Cytogenetic Dosimetry

Rj, DuFrain; Lg, Littlefield; Ee, Joiner; El, Frome

doi:10.1097/00004032-197909000-00002

Cited by 37 publications

(4 citation statements)

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“…The biological plausibility for this KER is strong, as there is a broad mechanistic understanding of the process CA induction from deposited energy in the form of radiation, which is widely accepted. Many studies have provided clear evidence to support this KER using both in vitro and in vivo models Cheki et al 2016;Mcmahon et al 2016;Puig et al, 2016;Curwen et al, 2012;Testa et al, 2018;Cornforth et al, 2002;Loucas et al, 2013;Nagasawa et al, 1990a;Edwards et al, 1980;Themis et al, 2013;Schmid et al, 1996;Mestres et al, 2004;Bilbao et al, 1989;Mill et al, 1996;Brooks, 1975;Durante et al, 1992;Takatsuji and Sasaki, 1984;Moquet et al, 2001;Purrott et al, 1980;duFrain et al, 1979).…”

Section: Biological Plausibilitymentioning

confidence: 98%

“…Results from many studies indicate dose/incidence and temporal concordance between the deposition of energy and the increased frequency of chromosomal aberrations. There is strong evidence of a dose-dependent increase in a wide range of chromosomal aberrations in response to increasing radiation dose , Tucker 2005A, Tucker 2005B, Arlt 2014, Qian 2015Puig et al, 2016;Curwen et al, 2012;Testa et al, 2018;Cornforth et al, 2002;Loucas et al, 2013;Nagasawa et al, 1990a;Edwards et al, 1980;Themis et al, 2013;Schmid et al, 1996;Mestres et al, 2004;Bilbao et al, 1989;Mill et al, 1996;Brooks, 1975;Durante et al, 1992;Takatsuji and Sasaki, 1984;Moquet et al, 2001;Purrott et al, 1980;duFrain et al, 1979). Temporally, it is well-established that chromosomal aberrations occur after exposure to radiation , Tucker 2005A, Tucker 2005B, Abe 2018, though the exact timing is difficult to pinpoint because most assays take place hours or days after the radiation exposure.…”

Section: Deposition Of Energy (Mie) --> Chromosomal Aberrations Incre...mentioning

confidence: 99%

“…The evidence presented below is summarized in table 3, here (click link). In general, there is much evidence that deposition of energy by ionizing radiation results in a higher burden of CAs Cheki et al 2016;Mcmahon et al 2016;Puig et al, 2016;Curwen et al, 2012;Testa et al, 2018;Cornforth et al, 2002;Loucas et al, 2013;Nagasawa et al, 1990a;Edwards et al, 1980;Themis et al, 2013;Schmid et al, 1996;Mestres et al, 2004;Bilbao et al, 1989;Mill et al, 1996;Brooks, 1975;Durante et al, 1992;Takatsuji and Sasaki, 1984;Moquet et al, 2001;Purrott et al, 1980;duFrain et al, 1979). Reviews have been published that provide details regarding the relationships between radiation of different LETs and the relative effectiveness of CA induction , ionizing radiation and genomic instability , and low-dose ionizing radiation and chromosomal translocations (Tucker 2008).…”

Section: Empirical Evidencementioning

confidence: 99%

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Adverse Outcome Pathway on deposition of energy leading to lung cancer

2023

OECD Series on Adverse Outcome Pathways

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Despite its widespread recognition in chemical toxicology, the adverse outcome pathway (AOP) framework has not been fully explored in the radiation field to guide relevant research and subsequent risk assessment. Development of a radiation relevant AOP is described here using a case example of lung cancer. Lung cancer is a major public health problem world-wide, causing the deaths of an estimated 1.5 million people annually; it imposes a major health-care burden. Numerous environmental factors are known contributors including both chemical (e.g. asbestos, air pollution and arsenic) and radiation stressors (e.g. radon gas). Radon gas is the second leading cause of lung cancer in North America. Evidence suggests that environmental and indoor radon exposure constitutes a significant public health problem. The mechanism of lung cancer development from exposure to radon gas is unclear. Data suggest that cytogenetic damage from radon decay progeny may be an important contributor. This AOP defines a path to cancer using key events related to DNA damage response and repair. The molecular initiating event (MIE) which represents the first chemical interaction with the cell is identified as the deposition of ionizing energy. Energy deposited onto a cell can lead to multiple ionization events to targets such as DNA. This energy will break DNA double strands (KE1) and initiate double strand break (DSB) repair machinery. In higher eukaryotes, this occurs through nonhomologous end joining (NHEJ) which is a quick and efficient, but error-prone process (KE2). If DSBs occur in regions of the DNA transcribing critical genes, then mutations (KE3) generated through faulty repair may alter the function of these genes or may cause chromosomal aberrations (KE4), resulting in genomic instability. These events will alter the functions of many gene products and impact cellular pathways such as cell growth, cell cycling, and apoptosis. With these alterations, cell proliferation (KE5) will be promoted by escaping the regulatory control and form hyperplasia in lung epithelial cells, leading eventually to lung cancer (AO) induction and metastasis. The overall weight of evidence for this AOP is strong. The uncertainties and inconsistencies surrounding this AOP are centred on dose-response relationships associated with dose, dose-rates and radiation quality. The proposed AOP will act as a case example to motivate more researchers in the radiation field to use the AOP framework to effectively exchange knowledge and identify research gaps in the area of low dose risk assessment. 5 ContentsForeword .

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Section: Biological Plausibilitymentioning

confidence: 98%

Section: Deposition Of Energy (Mie) --> Chromosomal Aberrations Incre...mentioning

confidence: 99%

Section: Empirical Evidencementioning

confidence: 99%

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Adverse Outcome Pathway on deposition of energy leading to lung cancer

2023

OECD Series on Adverse Outcome Pathways

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“…Just like any other type of cancer, leukemia is a result from the somatic mutations of the DNA that activate or deactivate the tumor suppressor genes. These may occur suddenly or as a result of being exposed to radiation or carcinogenic substances that are influenced by the genetic factor [1]. Radiation exposure can be acute or chronic, and the severity of symptoms depends on many factors, such as total dose, dose rate, distribution of dose, susceptibility of the person to radiation, and the type of organs (more radiosensitive tissues) [2,3].…”

Section: Introductionmentioning

confidence: 99%

Radiation Exposure of Leukemia Blood Samples and Its Impacts on the Density of RBC, WBC, and PLT: <i>In Vitro</i>

Ismail¹,

Hamad²,

Harki³

2012

OJBIPHY

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Complete blood counts were analyzed for 12 samples (six males & six females: Ages 15 -40 years) of leukemia blood Samples for different dose rate and time of exposure using a Radium-226 source. Thus, an optimum time of exposure and exposure dose rate has improved for leukemia blood samples. Blood samples fractionated and placed in plastic wills, and melodic Coulter used to analysis exposed leukemia blood samples before and after exposure. Exposure technique involving CR-39 nuclear track detector and radiation survey dosimeter were used to estimate the alpha particle density incident on the blood samples and the exposed dose rate, respectively. In the first part, density of the accumulation of alpha particle on the surface of leukemia blood samples, and on the surface of CR-39NTDs varies exponentially with the exposed dose rate. This depends on the restricted energy loss of the incident alpha particles and target density. Assess an optimum time of exposure dose rate (1100 µSv/h) was the second objective. This depended on the changes in the blood components (PLT, WBC, and RBC) due to irradiation occurred for different durations of irradiation, and the duration of irradiation that influenced the leukemia blood samples (1 Male, 16 years and one Female 17 years) in this research was five minutes. Changes in the density of PLT, WBC, and RBC for leukemia blood samples and for different male (five males) and female (five females) was the third part of this research. It was found that the changes were variables due to the exposed dose rate. Optimum exposed dose rate to make more effects on the cancer cells for the leukemia blood samples began at the radiation dose rate of 43.25  1.206 µSv/h for both; male and female relatively, and this due to chromosomal aberration of the exposed cells. Finally, comparison study with the healthy blood samples has been investigated. More details are listed and clarified in the tables and figures of this paper.

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Comparison of radon‐daughter‐induced effects in repair‐proficient and repair‐deficient cho cell lines

Schwartz

Shadley

Atcher

et al. 1990

Environ and Mol Mutagen

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The radiobiological effects of the radon daughter 212Bi were investigated in the Chinese hamster ovary cell line AA8 and its radiosensitive derivative EM9. EM9 cells rejoin radiation-induced DNA strand breaks more slowly than do AA8 cells. Three endpoints were examined: cell killing, G2-induced chromosome aberration frequency, and mutation induction at the hypoxanthine (guanine) phosphoribosyltransferase (HGPRT) locus. Cells were exposed to the alpha-emitter 212Bi chelated to diethylenetriaminepentaacetic acid (212Bi-DTPA). As expected, 212Bi-DTPA was more effective than X-rays in producing cytotoxicity, chromosome aberrations, and gene mutations. The relative biological effectiveness (RBE) for all three endpoints ranged from about 2 for chromosome aberrations to 4.4 for mutation induction. EM9 was more sensitive than AA8 cells to the cytotoxic and clastogenic effects of both X-rays and 212Bi-DTPA, suggesting that the repair deficiency in EM9 cells affects response to low- and high-linear energy transfer (LET) radiation for these endpoints. There was no significant difference between these two cell lines in their mutagenic response to X-rays and AA8 was slightly more sensitive to the mutagenic effects of alpha radiation. These results suggest that alterations in DNA repair ability may affect response of cells to both low- and high-LET radiation-induced cytotoxicity and clastogenicity, but they appear to have little effect on gene mutation induction.

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Human Cytogenetic Dosimetry

Cited by 37 publications

References 1 publication

Adverse Outcome Pathway on deposition of energy leading to lung cancer

Adverse Outcome Pathway on deposition of energy leading to lung cancer

Radiation Exposure of Leukemia Blood Samples and Its Impacts on the Density of RBC, WBC, and PLT: <i>In Vitro</i>

Comparison of radon‐daughter‐induced effects in repair‐proficient and repair‐deficient cho cell lines

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Human Cytogenetic Dosimetry

Cited by 37 publications

References 1 publication

Adverse Outcome Pathway on deposition of energy leading to lung cancer

Adverse Outcome Pathway on deposition of energy leading to lung cancer

Radiation Exposure of Leukemia Blood Samples and Its Impacts on the Density of RBC, WBC, and PLT: &lt;i&gt;In Vitro&lt;/i&gt;

Comparison of radon‐daughter‐induced effects in repair‐proficient and repair‐deficient cho cell lines

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Radiation Exposure of Leukemia Blood Samples and Its Impacts on the Density of RBC, WBC, and PLT: <i>In Vitro</i>